475). On day 3, 12 patients had MES (7/25 on LMWH, 5/20 on aspirin; P= .821). On day 7, 11 patients had MES (6/25 on LMWH, 5/20 on aspirin; P= .938). The median of the number of MES on days 1, 3, and 7 was 4 (range 1-10), 5 (range 1-42), and 3 (range 1-33) for the LMWH group and 1 (range 1-15), 4 (range 1-10), and 2 (range 1-4) for the aspirin group. There were no significant differences in the frequency of MES between patients with large artery occlusive disease treated with LMWH and aspirin. “
“An important imaging technique that has advanced

decision-making for noninvasive preoperative evaluation is functional magnetic resonance imaging (fMRI). Preoperative fMRI imaging based AZD2281 on blood oxygenation level dependent (BOLD) fMRI is routinely used to map a variety of eloquent cortex brain functions such as language, visual, and sensory-motor regions. The purpose of this study was to evaluate the regional volumes of sensory and motor cortex (SMC) activation by two widely used fMRI motor tasks: a simple hand squeeze (HS) versus a more complex finger-to-thumb (FTT) opposition. Ten right-handed (five males; five females) subjects were studied using a block design BOLD fMRI technique at 1.5T. A region of interest analysis was performed in the right and left SMC following a HS and FTT task with the dominant right hand. Results show the total volume of motor and sensory

activation for ipsilateral and contralateral areas for the FTT task was statistically larger than the HS task (P= .02). Due to the greater U0126 manufacturer degree of activation of the SMC with the FTT task, we suggest use of this task over the HS task if a patient can adequately perform

the more complex FTT task. The greater SMC activation using FTT task compared to the HS task was primarily due to an increase in activation in the post-central sensory cortex. There was less lateralization, and therefore a greater degree of bilateral SMC activation, in the FTT task compared to the HS task. These results show the importance of optimization and fMRI task selection for presurgical SMC mapping. “
“White matter lesions (WMLs) are age-related manifestations of ischemic cerebrovascular disease and increase the risk for Alzheimer’s disease (AD). The apolipoprotein E (ApoE) ɛ4 allele is a risk factor for late onset AD and has selleck compound been related to low cerebrospinal fluid (CSF) Aβ42 levels and to cerebrovascular disease. The present study analyzed the relationship between WMLs, ApoE-ɛ4 genotype, and low CSF Aβ42. A total of 235 memory clinic attenders were stratified in 3 groups according to WML load. WMLs were rated on axial T2 magnetic resonance imaging images. Group 1 had no or only small amounts of periventricular (PV) or subcortical (SC) WMLs, WML group 2 had high amounts of PV WMLs and low amounts of SC WMLs, and WML group 3 had high amounts of both PV and SC WMLs.

475). On day 3, 12 patients had MES (7/25 on LMWH, 5/20 on aspirin; P= .821). On day 7, 11 patients had MES (6/25 on LMWH, 5/20 on aspirin; P= .938). The median of the number of MES on days 1, 3, and 7 was 4 (range 1-10), 5 (range 1-42), and 3 (range 1-33) for the LMWH group and 1 (range 1-15), 4 (range 1-10), and 2 (range 1-4) for the aspirin group. There were no significant differences in the frequency of MES between patients with large artery occlusive disease treated with LMWH and aspirin. “
“An important imaging technique that has advanced

decision-making for noninvasive preoperative evaluation is functional magnetic resonance imaging (fMRI). Preoperative fMRI imaging based NVP-LDE225 ic50 on blood oxygenation level dependent (BOLD) fMRI is routinely used to map a variety of eloquent cortex brain functions such as language, visual, and sensory-motor regions. The purpose of this study was to evaluate the regional volumes of sensory and motor cortex (SMC) activation by two widely used fMRI motor tasks: a simple hand squeeze (HS) versus a more complex finger-to-thumb (FTT) opposition. Ten right-handed (five males; five females) subjects were studied using a block design BOLD fMRI technique at 1.5T. A region of interest analysis was performed in the right and left SMC following a HS and FTT task with the dominant right hand. Results show the total volume of motor and sensory

activation for ipsilateral and contralateral areas for the FTT task was statistically larger than the HS task (P= .02). Due to the greater selleck screening library degree of activation of the SMC with the FTT task, we suggest use of this task over the HS task if a patient can adequately perform

the more complex FTT task. The greater SMC activation using FTT task compared to the HS task was primarily due to an increase in activation in the post-central sensory cortex. There was less lateralization, and therefore a greater degree of bilateral SMC activation, in the FTT task compared to the HS task. These results show the importance of optimization and fMRI task selection for presurgical SMC mapping. “
“White matter lesions (WMLs) are age-related manifestations of ischemic cerebrovascular disease and increase the risk for Alzheimer’s disease (AD). The apolipoprotein E (ApoE) ɛ4 allele is a risk factor for late onset AD and has selleck been related to low cerebrospinal fluid (CSF) Aβ42 levels and to cerebrovascular disease. The present study analyzed the relationship between WMLs, ApoE-ɛ4 genotype, and low CSF Aβ42. A total of 235 memory clinic attenders were stratified in 3 groups according to WML load. WMLs were rated on axial T2 magnetic resonance imaging images. Group 1 had no or only small amounts of periventricular (PV) or subcortical (SC) WMLs, WML group 2 had high amounts of PV WMLs and low amounts of SC WMLs, and WML group 3 had high amounts of both PV and SC WMLs.

We have known for a long time that HRS represented a spectrum of pathology and pathophysiology, and this culminated in the publication in 1996 of the new criteria for the definition of HRS by the International Ascites Club of type 1 HRS and type 2 HRS.1 Without going into the definitions,

in essence type 1 HRS is the rapid onset of renal failure that occurs in patients with rapid decompensation of cirrhosis due to either alcoholic hepatitis, or acute on chronic liver failure, or acute liver failure. Type 2 HRS is the type of renal impairment observed in patients with refractory ascites, with renal function fluctuating over a relatively long period of time. This definition was born out of necessity, mainly to facilitate research check details in the area since, prior to this date, patients tended to be clumped together when it was clear that clinically and presumably their underlying pathophysiology were different. ABT 263 While these definitions have helped us move on in terms of identifying mechanisms, the definitions have by virtue of their criteria probably held us back, by identifying patients late, and with relatively advanced renal

failure. Thus, the definitions involve absolute serum creatinine values which we now know are inappropriate. Thus, a serum creatinine in a heavily built black muscular man are treated the same as an emaciated white female with advanced alcoholic liver disease. This definition bit us back when two clinical trials of terlipressin in HRS showed a response rate to treatment of 34%-40%,2, 3 probably because patients were randomized too late for true efficacy. We are now seeing articles that state predictability of response to terlipressin is determined by serum creatinine.4 Another way of putting this is that patients with early HRS respond better to treatment than patients

with advanced kidney failure. In many ways this is “kind of obvious,” so we need new criteria that can be adapted to individual patients. This was also recognized in the working party report of Wong et al.5 The development of HRS is due to four main factors. These are: (1) altered systemic hemodynamics with vasodilatation and lowering of arterial pressure; (2) activation of the sympathetic nervous system, click here which alters renal autoregulation such that renal blood flow becomes more dependent on arterial pressure; (3) a terminal decline in cardiac function due to cirrhotic cardiomyopathy, which renders patients unable to maintain an adequate cardiac output as they decompensate; and (4) increased circulating or intrarenal vasoactive mediators, the role of which remain unknown. Importantly, the role of each of these factors probably varies from patient to patient. The advent of the new definition of acute kidney injury (AKI) by the AKI network has led to a reevaluation and proposed new definitions for HRS.5 What is well recognized by all is that current criteria for HRS recognize and treat patients too late.

We have known for a long time that HRS represented a spectrum of pathology and pathophysiology, and this culminated in the publication in 1996 of the new criteria for the definition of HRS by the International Ascites Club of type 1 HRS and type 2 HRS.1 Without going into the definitions,

in essence type 1 HRS is the rapid onset of renal failure that occurs in patients with rapid decompensation of cirrhosis due to either alcoholic hepatitis, or acute on chronic liver failure, or acute liver failure. Type 2 HRS is the type of renal impairment observed in patients with refractory ascites, with renal function fluctuating over a relatively long period of time. This definition was born out of necessity, mainly to facilitate research Selleckchem Small molecule library in the area since, prior to this date, patients tended to be clumped together when it was clear that clinically and presumably their underlying pathophysiology were different. Everolimus molecular weight While these definitions have helped us move on in terms of identifying mechanisms, the definitions have by virtue of their criteria probably held us back, by identifying patients late, and with relatively advanced renal

failure. Thus, the definitions involve absolute serum creatinine values which we now know are inappropriate. Thus, a serum creatinine in a heavily built black muscular man are treated the same as an emaciated white female with advanced alcoholic liver disease. This definition bit us back when two clinical trials of terlipressin in HRS showed a response rate to treatment of 34%-40%,2, 3 probably because patients were randomized too late for true efficacy. We are now seeing articles that state predictability of response to terlipressin is determined by serum creatinine.4 Another way of putting this is that patients with early HRS respond better to treatment than patients

with advanced kidney failure. In many ways this is “kind of obvious,” so we need new criteria that can be adapted to individual patients. This was also recognized in the working party report of Wong et al.5 The development of HRS is due to four main factors. These are: (1) altered systemic hemodynamics with vasodilatation and lowering of arterial pressure; (2) activation of the sympathetic nervous system, selleck chemical which alters renal autoregulation such that renal blood flow becomes more dependent on arterial pressure; (3) a terminal decline in cardiac function due to cirrhotic cardiomyopathy, which renders patients unable to maintain an adequate cardiac output as they decompensate; and (4) increased circulating or intrarenal vasoactive mediators, the role of which remain unknown. Importantly, the role of each of these factors probably varies from patient to patient. The advent of the new definition of acute kidney injury (AKI) by the AKI network has led to a reevaluation and proposed new definitions for HRS.5 What is well recognized by all is that current criteria for HRS recognize and treat patients too late.

Hayashi et al.: Surg Today. 2014). However, the efficacy for preventing pulmonary embolism (PE) after HBP surgery is still unclear. Methods: To assess the rate of VTE and hemorrhage after elective HBP surgery, as a general rule, enoxaparin or fondaparinux for postoperative thromboprophylaxis was administered from January 2009 to December 2012 (former period), whereas it was not administered from January 2013 to June 2014 (latter

period). In former and latter period, 366 of 490 (74.4%) and 8 of 161 (5%) patients received chemical thromboprophylaxis at the chief surgeon’s discretion, respectively. Results: VTE and PE were occurred to 29 (5.9%) and 5 (1.0%) patients in former period, and were occurred LBH589 cost to 11 (6.8%) and 6 (3.7%) patients in

latter period, respectively. Administration of chemical thromboprophylaxis TGF-beta inhibitor did not decrease VTE rate compared with non-administrated patients (4.8% vs 7.9%, respectively, p = 0.1025), but PE rate was significantly high in non-administration group (0.8% vs 2.9%, p = 0.0410). Postoperative hemorrhage was occurred at significantly high rate in administration group (23.9% vs 10.6%, p = 0.0001), but the rate of major hemorrhage, which required blood transfusion or hemostasis with surgery or IVR technique, was equivalent in both groups (5.9% vs 8.3%, click here p = 0.2313). Logistic regression analysis showed age 69 or over is significant risk factor of VTE (p = 0.0091, odds ratio (OR): 2.40, 95% CI: 1.24–4.78) and PE (p = 0.0466, odds ratio (OR): 3.63, 95% CI: 1.02–16.96). Non-administration of chemical prophylaxis also significantly increased the risk of PE (p = 0.0433, odds ratio (OR): 3.67, 95% CI: 1.04–17.00). Conclusion: Administration of chemical thromboprophylaxis after

HBP surgery is safe and beneficial because it did not increase the major hemorrhage risk and decreases the risk of PE. Key Word(s): 1. venous thromboembolism; 2. pulmonary embolism; 3. thromboprophylaxis; 4. hepatobiliary-pancreatic surgery Presenting Author: KIYOSHI HIRAMATSU Additional Authors: TOSHIYUKI ARAI, SATOMI SAEKI, TAKESHI AMEMIYA, HIDENARI GOTO, TAKASHI SEKI Corresponding Author: KIYOSHI HIRAMATSU Affiliations: Anjo Kosei Hospital, Anjo Kosei Hospital, Anjo Kosei Hospital, Anjo Kosei Hospital, Anjo Kosei Hospital Objective: Major surgery for hemodialysis patients with nephropathy seems to be at high risk. In this report we analyzed short term outcome (postoperative mortality and morbidity) and long term outcome (over all survival) of the surgery for gastric cancer in patients with nephropathy under the maintenance of hemodialysis.

Hayashi et al.: Surg Today. 2014). However, the efficacy for preventing pulmonary embolism (PE) after HBP surgery is still unclear. Methods: To assess the rate of VTE and hemorrhage after elective HBP surgery, as a general rule, enoxaparin or fondaparinux for postoperative thromboprophylaxis was administered from January 2009 to December 2012 (former period), whereas it was not administered from January 2013 to June 2014 (latter

period). In former and latter period, 366 of 490 (74.4%) and 8 of 161 (5%) patients received chemical thromboprophylaxis at the chief surgeon’s discretion, respectively. Results: VTE and PE were occurred to 29 (5.9%) and 5 (1.0%) patients in former period, and were occurred Gefitinib to 11 (6.8%) and 6 (3.7%) patients in

latter period, respectively. Administration of chemical thromboprophylaxis GSK1120212 nmr did not decrease VTE rate compared with non-administrated patients (4.8% vs 7.9%, respectively, p = 0.1025), but PE rate was significantly high in non-administration group (0.8% vs 2.9%, p = 0.0410). Postoperative hemorrhage was occurred at significantly high rate in administration group (23.9% vs 10.6%, p = 0.0001), but the rate of major hemorrhage, which required blood transfusion or hemostasis with surgery or IVR technique, was equivalent in both groups (5.9% vs 8.3%, click here p = 0.2313). Logistic regression analysis showed age 69 or over is significant risk factor of VTE (p = 0.0091, odds ratio (OR): 2.40, 95% CI: 1.24–4.78) and PE (p = 0.0466, odds ratio (OR): 3.63, 95% CI: 1.02–16.96). Non-administration of chemical prophylaxis also significantly increased the risk of PE (p = 0.0433, odds ratio (OR): 3.67, 95% CI: 1.04–17.00). Conclusion: Administration of chemical thromboprophylaxis after

HBP surgery is safe and beneficial because it did not increase the major hemorrhage risk and decreases the risk of PE. Key Word(s): 1. venous thromboembolism; 2. pulmonary embolism; 3. thromboprophylaxis; 4. hepatobiliary-pancreatic surgery Presenting Author: KIYOSHI HIRAMATSU Additional Authors: TOSHIYUKI ARAI, SATOMI SAEKI, TAKESHI AMEMIYA, HIDENARI GOTO, TAKASHI SEKI Corresponding Author: KIYOSHI HIRAMATSU Affiliations: Anjo Kosei Hospital, Anjo Kosei Hospital, Anjo Kosei Hospital, Anjo Kosei Hospital, Anjo Kosei Hospital Objective: Major surgery for hemodialysis patients with nephropathy seems to be at high risk. In this report we analyzed short term outcome (postoperative mortality and morbidity) and long term outcome (over all survival) of the surgery for gastric cancer in patients with nephropathy under the maintenance of hemodialysis.

With respect to treatment duration among patients with HCV RNA negativiation during re-treatment, 72 weeks of treatment significantly increased the SVR rate compared to 48 weeks. This result was almost the same as that of the REPEAT study.16 In our present study, the SVR rate among the patients with c-EVR but not RVR in re-treatment was significantly high by 72 weeks of treatment. On the other hand, the SVR rates among the patients with RVR in re-treatment were similar between the patients with 48 weeks and 72 weeks of treatment. Thus, patients with c-EVR

but not RVR in re-treatment should be re-treated for a longer period. In order to attain better SVR, extended treatment duration is generally recommended for patients with on-treatment LVR, whereas standard treatment duration Erlotinib ic50 is considered to be sufficient for patients with on-treatment c-EVR. However, the present study revealed that, even if patients achieved c-EVR on re-treatment, 72 weeks

of treatment seems to be better than 48 weeks for treatment-experienced patients. The majority of naïve patients showing on-treatment Ponatinib mouse c-EVR could eradicate HCV with 48 weeks of treatment while some could not. In a treatment-experienced setting, patients who are able to respond early but not eradicate HCV would be selected, and therefore extended treatment may be needed. With genotype 2, the SVR rate was relatively high (63%). The patients who could not attain SVR in re-treatment (two patients) showed NR in the previous treatment. Thus, the patients with genotype 2 and showing NR in previous treatment seemed to be difficult find more to treat and could be treated with other drugs. Among the patients with RVR in re-treatment, the SVR rates were similar among those with RVR in re-treatment between 24 weeks and 48 weeks of treatment. The effectiveness of extended treatment for the patients with genotype 2 in re-treatment could not be demonstrated because of their small number in this study. Further investigation is needed to clarify this. In conclusion, this study shows that the efficacy of re-treatment

for genotype 1 patients who failed to show SVR to previous treatment with PEG IFN plus ribavirin could be predicted from the previous treatment response and a low HCV RNA level at the start of re-treatment. Re-treatment for 72 weeks led to clinical improvement for genotype 1 patients with c-EVR and without RVR on re-treatment. THIS WORK WAS supported by a Grant-in-Aid for Research on Hepatitis from Ministry of Health Labor and Welfare of Japan, and Scientific Research from the Ministry of Education, Science, and Culture of Japan. “
“Endotoxin-mediated proinflammatory cytokines play a significant role in the pathogenesis of acute and chronic liver diseases. Heat shock protein 90 (molecular weight, 90 kDa) (hsp90) functions as an important chaperone of lipopolysaccharide (LPS) signaling and is required for the production of proinflammatory cytokines.

Together, we anticipate that full coverage sequencing (coding and noncoding sequences) of all known components of the telomerase enzyme complex and the shelterin complex of telomere-binding proteins will reveal an increasing percentage of telomere-related mutations in human cirrhosis. It remains

to be analyzed whether TERT mutations influence the development of HCC. Cirrhosis represents one of the main risk factors for HCC formation. There is ample evidence that telomere shortening increases the risk of cancer formation in humans by inducing chromosomal instability. Therefore, TERT mutations that increase the risk of cirrhosis formation may increase the risk of HCC. In contrast, tumor cells need to activate telomere maintenance mechanisms in order to gain immortal growth capacity—a prerequisite for tumor formation. Thus, it is possible that TERT mutations could also protect individuals from cancer Selleckchem PARP inhibitor formation.

In the current cohort, 5/14 (36%) cirrhosis patients with telomerase mutations (including one patient with a homozygous p.G1109R TERT mutation) developed HCC, indicating that telomerase mutations did not prevent cancer formation. Together, the current findings represent the first evidence for telomerase mutations in cirrhosis induced Selleckchem Olaparib by chronic liver disease. The results indicate that telomerase mutations represent confounding factors increasing the risk of cirrhosis formation in the context of chronic liver disease. The study results improve our understanding on the molecular causes of cirrhosis. These findings will influence the future development learn more of molecular therapies for cirrhosis patients and may also have an impact on future surveillance programs and decision making in treatment of patients with chronic liver disease and cirrhosis. Additional Supporting Information may be found in the online version of this article. “
“Sodium valproate (VPA) is widely used throughout the world to treat epilepsy, migraine, chronic headache, bipolar disorder, and as adjuvant chemotherapy.

VPA toxicity is an uncommon but potentially fatal cause of idiosyncratic liver injury. Rare mutations in POLG, which codes for the mitochondrial DNA polymerase γ (polγ), cause Alpers-Huttenlocher syndrome (AHS). AHS is a neurometabolic disorder associated with an increased risk of developing fatal VPA hepatotoxicity. We therefore set out to determine whether common genetic variants in POLG explain why some otherwise healthy individuals develop VPA hepatotoxicity. We carried out a prospective study of subjects enrolled in the Drug Induced Liver Injury Network (DILIN) from 2004 to 2008 through five US centers. POLG was sequenced and the functional consequences of VPA and novel POLG variants were evaluated in primary human cell lines and the yeast model system Saccharomyces cerevisiae.

Together, we anticipate that full coverage sequencing (coding and noncoding sequences) of all known components of the telomerase enzyme complex and the shelterin complex of telomere-binding proteins will reveal an increasing percentage of telomere-related mutations in human cirrhosis. It remains

to be analyzed whether TERT mutations influence the development of HCC. Cirrhosis represents one of the main risk factors for HCC formation. There is ample evidence that telomere shortening increases the risk of cancer formation in humans by inducing chromosomal instability. Therefore, TERT mutations that increase the risk of cirrhosis formation may increase the risk of HCC. In contrast, tumor cells need to activate telomere maintenance mechanisms in order to gain immortal growth capacity—a prerequisite for tumor formation. Thus, it is possible that TERT mutations could also protect individuals from cancer Rucaparib manufacturer formation.

In the current cohort, 5/14 (36%) cirrhosis patients with telomerase mutations (including one patient with a homozygous p.G1109R TERT mutation) developed HCC, indicating that telomerase mutations did not prevent cancer formation. Together, the current findings represent the first evidence for telomerase mutations in cirrhosis induced CSF-1R inhibitor by chronic liver disease. The results indicate that telomerase mutations represent confounding factors increasing the risk of cirrhosis formation in the context of chronic liver disease. The study results improve our understanding on the molecular causes of cirrhosis. These findings will influence the future development selleck inhibitor of molecular therapies for cirrhosis patients and may also have an impact on future surveillance programs and decision making in treatment of patients with chronic liver disease and cirrhosis. Additional Supporting Information may be found in the online version of this article. “
“Sodium valproate (VPA) is widely used throughout the world to treat epilepsy, migraine, chronic headache, bipolar disorder, and as adjuvant chemotherapy.

VPA toxicity is an uncommon but potentially fatal cause of idiosyncratic liver injury. Rare mutations in POLG, which codes for the mitochondrial DNA polymerase γ (polγ), cause Alpers-Huttenlocher syndrome (AHS). AHS is a neurometabolic disorder associated with an increased risk of developing fatal VPA hepatotoxicity. We therefore set out to determine whether common genetic variants in POLG explain why some otherwise healthy individuals develop VPA hepatotoxicity. We carried out a prospective study of subjects enrolled in the Drug Induced Liver Injury Network (DILIN) from 2004 to 2008 through five US centers. POLG was sequenced and the functional consequences of VPA and novel POLG variants were evaluated in primary human cell lines and the yeast model system Saccharomyces cerevisiae.

Studies in nonhuman primates have been of major importance for experimental studies of human hepatitis viruses, including analyses of hepatitis A virus in New World monkeys (tamarins and owl monkeys), HBV, hepatitis D virus, and hepatitis C virus (HCV) in hominoids (chimpanzees), and hepatitis E virus in Old World monkeys (cynomolgus and rhesus macaques).[2-5] Chimpanzees are the only animal SP600125 datasheet model for studies of human HBV and HCV infections and related innate and adaptive host immune responses.[6] Chimpanzees have been available primarily for research in the United States, where several animal facilities

can perform studies in a suitable environment. However, a report from the Institute of Medicine (released December 15, 2011), evaluating the role of this model in biomedical research, has limited or eliminated most experimental research in chimpanzees funded by the National Institutes of Health, a major funding agency for such research.[7] The use of buy Ribociclib chimpanzees for persistent HBV was already rather limited because the chronicity rate in experimental infections is low, and only a small number of animals have been available. Cost has been another limiting factor. However, a recent study by Lanford

et al. showed how the chimpanzee model could be used to determine the effect of molecules affecting pathways of the immune system; it was demonstrated that a Toll-like receptor 7 agonist could effectively lower HBV viral load partly by inducing antigen-specific T- and natural killer cell responses.[8] New World monkeys (e.g., tamarins, marmosets, and owl and spider monkeys commonly used in biomedical research) do not appear to be susceptible

to human HBV. An HBV variant was identified in Woolly monkeys (endangered species) and could lead to acute, but not persistent, experimental infection in Spider monkeys.[9, 10] Among Old World selleckchem monkeys, there is evidence of occult human HBV infection of subgenotype A2 in baboons with detection of the HBV DNA genome at low titers in serum, but not the HBV surface antigen (HBsAg).[11] However, HBV could be transmitted to naïve baboons and HBV DNA could be detected for at least 6 months. It remains to be determined whether this will be a relevant model for studying chronic HBV infection. Cynomolgus and rhesus macaques are frequently used in biomedical research, but it has been unclear whether human HBV could be transmitted to these animals. The possibility of using rhesus monkeys for experimental human HBV infection was examined early after the discovery of HBV. Thus, in 1972, London et al. reported that HBV could be transmitted to rhesus monkeys (Macaca mulatta) and serially passaged to naïve monkeys, but this could not be confirmed subsequently.[12] In 2002, Gheit et al. reported that Barbary apes (M.